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 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Severe necrotizing pancreatitis is accompanied by release of hemorrhagic ascites fluid (HAF), which is thought to be related to the occurrence and frequency of cardiocirculatory and pulmonary failure as a consequence of acute pancreatitis. The purpose of this study was to evaluate the role of HAF due to these systemic complications. Experiments were performed in 25 pigs (mean b.wt. 22 +/- 1 kg) under general anesthesia and mechanical ventilation. The animals received 50 ml/kg b.wt. i.p. of either physiologic saline solution (control CO, n = 9) or hemorrhagic ascites fluid (HAF, n = 16). HAF was obtained from 16 pigs with pancreatitis induced by intraductal infusion of bile salt. Eight animals in the HAF group were pretreated with indomethacin (10 mg/kg i.v. INDO/HAF). All animals were followed up for 6 h. Mean arterial pressure, cardiac output, and stroke volume fell significantly in the HAF (-25%, -27%, -27%) and in the INDO/HAF groups (-24%, -20%, -17%) as compared with controls (-6%, -6%, -6%). Also, left ventricular end-diastolic pressure (LVEDP) decreased by 52% and 48% in both HAF recipient groups, whereas LVEDP was unchanged in the control group. Myocardial contractility (Vmax) remained unaltered in all experimental groups. No significant differences in gas exchange and lung dry/wet weight ratio were observed. Lipase and PGI2 of the unpretreated HAF group rised to 203% and 198% in arterial blood at 6 h compared with unaltered levels in the control group. No increase of prostanoid concentrations was detected in the indomethacin-pretreated group, whereas lipase increase by a comparable extent as in the HAF group. We conclude that the early consequences of HAF are mainly characterized by systemic hypotension due to hypovolemia.
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PMID:Hemodynamic effects following intraperitoneal infusion of pancreatic ascites fluid. 141 Aug 1

Acute pancreatitis was induced in 19 anesthetized dogs by retrograde injection of bile mixed with trypsin into the pancreatic duct. Two groups, of six animals each, were treated with intravenous infusion of synthetic antiproteases: gabexate mesilate and nafamostat mesilate in doses of 1 mg/kg per hr. One group of seven animals remained untreated. Two untreated dogs died during the experiment. All the treated dogs survived. Hemodynamic data were monitored hourly during a 6-hr observation period. In the untreated animals, cardiac output, mean arterial pressure, and left ventricular stroke volume decreased rapidly; an increase of pulmonary vascular resistance and systemic vascular resistance was observed. Synthetic antiproteases, given as a therapy, improved the hemodynamic parameters significantly and prevented the animals from developing shock. Gabexate mesilate and nafamostat mesilate seem to be of value in the treatment of experimentally produced acute pancreatitis in dogs.
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PMID:Synthetic antiproteases in acute pancreatitis: an experimental study. 173 37

Acute pancreatitis was induced in 13 anesthetized dogs by retrograde injection of bile mixed with trypsin into the pancreatic duct. Six animals were treated with intravenous infusion of new synthetic antiprotease. Nafamostat Mesilate, at a dose of 1 mg/kg/h. Four out of seven untreated animals died during the experiment. All the treated dogs survived. Hemodynamic data were regularly monitored during a ten-hour observation period. Cardiac output, mean arterial pressure and left ventricular stroke volume decreased rapidly in the untreated animals. An increase in systemic vascular resistance and pulmonary vascular resistance was observed in dogs without treatment. Nafamostat Mesilate given as therapy significantly improved the hemodynamic parameters, and prevented the animals from developing shock. The study demonstrates an advantageous influence of synthetic antiprotease Nafamostat Mesilate on the course of acute experimental pancreatitis.
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PMID:Beneficial effect of therapeutic infusion of nafamostat mesilate (FUT-175) on hemodynamics in experimental acute pancreatitis. 185 71

Acute pancreatitis was induced in ten anesthetized dogs by retrograde injection for bile mixed with trypsin into the pancreatic duct. Five animals were treated with i.v. infusion of gabexate mesilate in a dose of 1 mg/kg per hour. Hemodynamic data were regulary monitored during a 10-h observation period. Cardiac output (CO), mean arterial pressure (MAP), and left ventricular stroke volume (LVSV) decreased rapidly in untreated animals. An increase of systemic vascular resistance (SVR) and pulmonary vascular resistance (PVR) was observed in dogs without treatment. Gabexate mesilate given as a therapy significantly improved the hemodynamic parameters. The study demonstrates an advantageous influence of synthetic antiprotease gabexate mesilate on the course of acute experimental pancreatitis.
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PMID:Effect on hemodynamics of therapeutic infusion of gabexate mesilate (FOY) in experimental acute pancreatitis. 249 22

The role of reactive oxygen metabolites in extrapancreatic organ dysfunction associated with acute hemorrhagic pancreatitis was studied in dogs. Experimental pancreatitis was induced by the intraductal infusion of activated trypsin and taurocholate. Cardiac output, pulmonary and systemic blood pressure, pulmonary wedge pressure, central venous pressure, heart rate, blood gases and serum amylase were measured. Cardiac index, pulmonary and systemic vascular resistance, and the right and left stroke work were calculated. Systemic arterial and venous blood pressure and cardiac index gradually declined over 6 hr, while pulmonary mean blood pressure and pulmonary vascular resistance increased. Pretreatment of pancreatitis with catalase and superoxide dismutase prevented the rise in mean pulmonary blood pressure, moderated the rise in pulmonary vascular resistance, and decreased the rate and extent of the fall in cardiac index. These data suggest that reactive oxygen metabolites may play some role in the extraabdominal organ manifestations of acute pancreatitis.
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PMID:Role of reactive oxygen metabolites in early cardiopulmonary changes of acute hemorrhagic pancreatitis. 279 9

The case histories of the 49 patients who died in a series of 165 patients admitted to the Medical Unit between 1958 and 1984 with polyarteritis nodosa (PAN) were reviewed. The causes of death of the 29 men and 20 women, mean age 51.44 +/- 7.4 years, were classified into 6 groups. Infection accounted for 26.5% (13/49) of deaths, the initial site of infection being pulmonary, complicated by septicaemia in 6 cases. Cardiovascular events were responsible for death in 24.4% (11/49): terminal cardiac failure (4 cases), myocardial infarction (1 case), ventricular tachycardia (1 case), stroke (1 case), pulmonary embolism (2 cases), fulminant hemoptysis (1 case). Gastrointestinal complications were the cause of death in 16.3% (8/49): ischemic necrosis (5 cases), acute pancreatitis (2 cases), oesophageal ulceration (1 case). Renal failure was observed in 10.2% (5/49), all occurring before 1972: acute renal failure (3 cases), chronic renal failure (2 cases). Cancer was the cause of death in 10.2% (5/49): primary bronchial carcinoma (2 cases), laryngeal carcinoma (1 case), carcinoma of the vulva (1 case), bone metastases (1 case). Finally, 14.2% (7/49) could not be classified in the preceding groups. Sudden death occurred in 3 patients, shock in 1 patient, multivisceral PAN in 2 patients and anaphylactic shock in 1 patient. Three of the 12 patients who had post-mortem studies had signs of progressive vasculitis. The results are compared with other reports in the literature and the pathogenic mechanisms are discussed. The infections and cardiovascular deaths occurred early or late and were not related to the state of the activity of the vasculitis. Immunosuppressive treatment seems to play an important role in their pathogenesis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Causes of death in systemic vasculitis of polyarteritis nodosa. Analysis of a series of 165 patients]. 290 28

The purpose of this study was to determine the incidence of death as the initial manifestation of cholelithiasis. Records of patients who died or underwent cholecystectomy for gallstone-related disease at Duke University Medical Center between 1976 and 1985 were reviewed. Thirty patients died, six of whom (20%) had previous episodes of biliary pain and stone documentation. Twenty-four (80%) were asymptomatic (three with previous incidental diagnosis of cholelithiasis). Reason for admission included acute cholecystitis (nine), pancreatitis (eight), biliary pain (six), cholangitis (four), jaundice (one), and endocarditis (one). Three patients died of gallstone complications without surgical intervention; one patient had renal failure and two had septicemia. Other causes of death were: sepsis (seven patients), cardiac failure (six), pulmonary complications (four), renal failure (three), cerebrovascular accident (three), liver failure (two), pancreatitis (one), and gastrointestinal bleeding (one). During this period, 1731 cholecystectomies were performed without mortality. In this group, the patients were younger (50 +/- 8 years vs. 64 +/- 13 years, p less than 0.001), and had a lower incidence of cirrhosis (p less than 0.001) and diabetes (p less than 0.002). The sex ratio was inverted (p less than 0.001). This study demonstrates that death from gallstones is uncommon (three cases per year), as is death from their initial clinical manifestation (1.2%). The risk of death is two- and ninefold higher in patients with acute cholecystitis or acute pancreatitis. Age, cirrhosis, and diabetes are important determinants of outcome.
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PMID:Deaths from gallstones. Incidence and associated clinical factors. 291 58

Acute pancreatitis is often associated with impaired cardiovascular function. This study examined the systemic cardiovascular effect of acute pancreatitis induced by injection of autologous bile (0.5 ml/kg) into the canine pancreatic duct. After acute pancreatitis was induced, eight dogs were given no resuscitation (group 1, untreated pancreatitis), and lactated Ringer's solution was infused in 11 dogs (group II, treated pancreatitis) to maintain mean arterial pressure and pulmonary wedge pressure at control values. In the untreated pancreatitis group, mean arterial pressure, cardiac output, stroke volume, and stroke work values decreased (mean arterial pressure from 101 +/- 4 to 74 +/- 12 mm Hg, cardiac output from 118 +/- 7 to 56.2 +/- 1.1 ml/min/kg; stroke volume from 0.93 +/- 0.08 to 0.22 +/- 0.07 ml/beat/kg; p less than 0.05), whereas heart rate and peripheral resistance increased (heart rate from 125 +/- 7 to 185 +/- 10 beats/min, peripheral vascular resistance from 3130 +/- 410 to 4436 +/- 610 dynes/sec/cm5; p less than 0.05). Although coronary blood flow, endocardial-epicardial flow ratio, and myocardial oxygen delivery values decreased progressively in group I after induction of pancreatitis, these changes did not achieve statistical significance. All indices of cardiovascular function and coronary blood flow remained unchanged in group II. Neither dP/dt max, the maximal rate of left ventricular pressure increase, nor dP/dt at a developed pressure of 40 mm Hg (an index of myocardial contractility minimally affected by changes in preload and afterload) were depressed by bile-induced acute canine pancreatitis in either group. Our data indicate that the detrimental effects of acute pancreatitis on cardiovascular function are related solely to hypovolemia and reduced cardiac filling and not to humoral or reflex effects induced by the disease.
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PMID:Hemodynamic function in acute pancreatitis. 328 79

The long-term clinical courses of 212 "cured" (normocalcemic) patients were analyzed for 1 to 25 years (mean, 6.8 +/- 5.4 years). Preoperatively, 181 patients (85%) were classified as having typical symptoms, 22 patients (11%) as having minimal symptoms, and nine patients (4%) as having no symptoms of primary hyperparathyroidism (PHP). Although the formation of urinary calculi was stopped in 91% of patients, deteriorated renal function and hypertension were seen in patients with symptoms (14% and 8%, respectively) and patients with minimal symptoms of PHP (6% and 15%, respectively). Renal function changes and hypertension were unpredictable despite normalization of the hyperactive parathyroid metabolism and had decisive results: 7% of the patients died of uremia or of the consequences of hypertension (stroke). Large, multiple bone lesions healed functionally and were of no prognostic significance. In the majority of patients with symptoms of PHP, gastrointestinal manifestations healed postoperatively, but two patients who had no preoperative gastrointestinal complaints died of acute pancreatitis. Almost all symptoms of the hypercalcemia syndrome disappeared immediately and permanently in patients with symptoms and patients with minimal symptoms of PHP. Neither deterioration of renal function nor elevation of blood pressure were observed postoperatively in "cured" patients who showed no symptoms of PHP preoperatively. Even in these patients, immediate surgical treatment may have avoided the complications of chronic renal failure or hypertension. As soon as organic manifestations, even in mild form, have been established, it seems impossible to predict the course and to prevent an unfavorable clinical outcome.
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PMID:Successful parathyroidectomy in primary hyperparathyroidism: a clinical follow-up study of 212 consecutive patients. 368 53

Physiologic abnormalities were evaluated by sequential hemodynamic and oxygen transport measurements in 33 patients with acute pancreatitis. The hypotensive crisis, which was defined as the lowest mean arterial pressure (MAP), was used as the common temporal reference point to align the data in a coherent fashion. The data of the 48-hour periods before and after the hypotensive crisis then were evaluated. The patients were divided into normotensive and hypotensive groups and the latter were divided into survivors and nonsurvivors to evaluate the severity of the disorder and to identify the patterns representative of survival and death. The physiologic abnormalities of the hypotensive patients include decreased systemic vascular resistance index (SVRI) and compromised cardiac function. The latter was demonstrated during the hypotensive episode by significantly reduced left ventricular stroke work index (LSWI), despite increases in heart rate (HR), central venous pressure (CVP), pulmonary capillary wedge pressure (WP), and cardiac index (CI). The normotensive group had increased oxygen consumption (Vo2), oxygen delivery (Do2), pulmonary shunt (Qsp/Qt), LSWI, normal SVRI, and high CI. The hypotensive nonsurvivors had lower MAP, LSWI, SVRI, Do, and hematocrit as well as higher pulmonary vascular resistance index (PVRI) and Qsp/Qt than did the survivors. These findings do not support myocardial depression as the primary cardiovascular abnormality in acute pancreatitis, but rather suggest the decreased vascular tone from flow maldistribution in the peripheral microcirculation limits tissue oxygenation in the face of increased metabolic requirements of the hypercatabolic state.
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PMID:Sequential hemodynamic and oxygen transport abnormalities in patients with acute pancreatitis. 670 89


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